prostaglandin-d2 and Hyperlipoproteinemias

It is generally accepted that in hyperlipoproteinemia (HLP) the vascular prostacyclin formation is diminished. We wondered, whether HLP is also associated with changes in platelet sensitivity to antiaggregatory prostaglandins. Therefore, we examined the platelet sensitivity to the prostaglandins PGI2 and PGD2 as well as plasma thromboxane B2 (TXB2)-levels in 24 patients with HLP type IIa, IIb and IV. We found a marked decrease of platelet sensitivity to PGI2 in all the patients examined, which was more pronounced in type IIb than in types IIa and IV. Platelet sensitivity to PGD2 showed no difference in the hyperlipemic patients. Plasma TXB2-levels were significantly increased in comparison to a control group, the changes being most pronounced in patients with type IV HLP. Platelet half-life was significantly shortened in the HLP-patients. This in-vivo platelet function parameter was found to be reduced in patients with type IIa HLP to the greatest extent. Our findings suggest that platelet deposition in HLP is promoted not only by diminished vascular PGI2-formation, but also by decreased sensitivity of the platelets to antiaggregatory prostaglandins. The high TXB2-levels and the shortened platelet half-life reflect the in-vivo activated platelet population in these patients.

Topics: Adult; Aged; Blood Platelets; Epoprostenol; Female; Half-Life; Humans; Hyperlipoproteinemia Type II; Hyperlipoproteinemia Type IV; Hyperlipoproteinemias; In Vitro Techniques; Male; Middle Aged; Platelet Aggregation; Prostaglandin D2; Prostaglandins D; Thromboxane B2

Platelet sensitivity to antiaggregatory prostaglandins (PGI2, PGE1, PGD2) was studied in 143 patients (122 male) with angiographically proven peripheral vascular disease and compared with age-matched clinically normal controls. Patients had a significantly lower platelet sensitivity to PGI2, PGE1, and PGD2 than controls. Clinical stages had no significant influence on the platelet sensitivity to PGI2 and PGE1. Patients with stage IIa had a lower sensitivity to PGD2 than patients with stage IV, the difference not being significant. Analyzing the influence of risk factors like diabetes, hyperlipoproteinemia, or smoking, there seemed to be an inverse relation between risk factors and platelet sensitivity to PGI2 and PGE1. Smokers especially, together with smokers exhibiting an additional risk factor, exhibited the highest prostaglandin consumption (PGI2, PGE1) and therefore the lowest platelet sensitivity. However, it has to be emphasized that the differences were not significant. There was a significant correlation between platelet sensitivity to PGI2 and PGE1, whereas this was not the case between the respective sensitivities to PGI2 and PGD2. This supports the hypothesis that both these prostaglandins (PGI2, PGE1) share the same receptor on the platelet surface, whereas PGD2 has its own receptor.

Topics: Adenosine Diphosphate; Aged; Alprostadil; Blood Platelets; Diabetes Mellitus; Epoprostenol; Female; Humans; Hyperlipoproteinemias; Male; Middle Aged; Platelet Aggregation; Prostaglandin D2; Prostaglandins D; Prostaglandins E; Risk; Smoking; Vascular Diseases